Cancer is one of the world’s most burdensome diseases, with increasing prevalence and a high mortality rate threat. Tumor recurrence and metastasis due to treatment resistance are two of the primary reasons that cancers have been so difficult to treat. The epithelial–mesenchymal transition (EMT) is essential for tumor drug resistance. EMT causes tumor cells to produce mesenchymal stem cells and quickly adapt to various injuries, showing a treatment-resistant phenotype. In addition, multiple signaling pathways and regulatory mechanisms are involved in the EMT, resulting in resistance to treatment and hard eradication of the tumors. The purpose of this study is to review the link between EMT, therapeutic resistance, and the molecular process, and to offer a theoretical framework for EMT-based tumor-sensitization therapy.

Bone formation occurs by two distinct mechanisms, namely, periosteal ossification and endochondral ossification. In both mechanisms, osteoblasts play an important role in the secretion and mineralization of bone-specific extracellular matrix. Differentiation and maturation of osteoblasts is a prerequisite to bone formation and is regulated by many factors. Recent experiments have shown that transcription factors play an important role in regulating osteoblast differentiation, proliferation, and function. Osteogenesis related transcription factors are the central targets and key mediators of the function of growth factors, such as cytokines. Transcription factors play a key role in the transformation of mesenchymal progenitor cells into functional osteoblasts. These transcription factors are closely linked with each other and in conjunction with bone-related signaling pathways form a complex network that regulates osteoblast differentiation and bone formation. In this paper, we discuss the structure of T-cell factor/lymphoid enhancer factor (TCF/LEF) and its role in embryonic skeletal development and the crosstalk with related signaling pathways and factors.

Bone defects caused by osteoporosis, bone malignant tumors, and trauma are very common, but there are many limiting factors in the clinical treatment of them. Bone tissue engineering is the most promising treatment and is considered to be the main strategy for bone defect repair. We prepared polydopamine-coated poly-(lactic-co-glycolic acid)/β-tricalcium phosphate composite scaffolds via 3D printing, and a series of characterization and biocompatibility tests were carried out. The results show that the mechanical properties and pore-related parameters of the composite scaffolds are not affected by the coatings, and the hydrophilicities of the surface are obviously improved. Scanning electron microscopy and micro-computed tomography display the nanoscale microporous structure of the bio-materials. Biological tests demonstrate that this modified surface can promote cell adhesion and proliferation and improve osteogenesis through the increase of polydopamine (PDA) concentrations. Mouse cranial defect experiments are conducted to further verify the conclusion that scaffolds with a higher content of PDA coatings have a better effect on the formation of new bones. In the study, the objective of repairing critical-sized defects is achieved by simply adding PDA as coatings to obtain positive results, which can suggest that this modification method with PDA has great potential.

Nanofibrous materials produced by electrospinning have attracted considerable attention from researchers in regenerative medicine. A combination of nanofibrous scaffold and chondrocytes is considered promising for repair of cartilage defect or damage. In the present study, we fabricated a poly(l-lactic-acid) (PLLA)/silk fibroin (SF) nanofibrous scaffold by electrospinning and evaluated its chondrogenic potential. The PLLA/SF nanofibers were characterized for diameter, surface wettability, swelling ratio, and tensile strength. Through in vitro experiments, PLLA/SF scaffold–chondrocyte interactions were investigated relative to the unmodified PLLA scaffold with regard to cellular adhesion, spreading, and proliferation by scanning electron microscopy and confocal laser scanning microscopy, and through analyses of DNA, sulfated glycosaminoglycan, and collagen. In addition, hematoxylin-eosin and Alcian blue-nuclear fast red staining were used to observe growth of chondrocytes, and secretion and distribution of cartilage-specific extracellular matrices in the scaffolds. Expressions of cartilage-related genes (collagen II, aggrecan, sox9, collagen I, and collagen X) were detected by real-time quantitative PCR. The PLLA/SF scaffold had better hydrophilicity, and could support chondrocytes adhesion and spreading more effectively than the unmodified PLLA scaffold. Chondrocytes secreted more cartilage-specific extracellular matrices and maintained their phenotype on the PLLA/SF scaffold. So it is concluded that the PLLA/SF scaffold is more conducive to in vitro formation of cartilage-like new tissues than the unmodified PLLA scaffold, and may be a promising material in cartilage tissue engineering.